Research Papers:

Pseudomonas aeruginosa-mannose-sensitive hemagglutinin inhibits pancreatic cancer cell proliferation and induces apoptosis via the EGFR pathway and caspase signaling

Xi Cheng, Bingrui Wang, Zhijian Jin, Ding Ma, Weiping Yang, Ren Zhao, Xiaoqian Jing, Baiyong Shen, Chenghong Peng and Weihua Qiu _

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Oncotarget. 2016; 7:77916-77925. https://doi.org/10.18632/oncotarget.12844

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Xi Cheng1,2,*, Bingrui Wang1,*, Zhijian Jin1,2,*, Ding Ma1,2, Weiping Yang1,2, Ren Zhao1,2, Xiaoqian Jing1,2, Baiyong Shen1,2, Chenghong Peng1,2, Weihua Qiu1,2

1Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China

2Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China

*These authors have contributed equally to this work

Correspondence to:

Weihua Qiu, email: [email protected]

Chenghong Peng, email: [email protected]

Baiyong Shen, email: [email protected]

Keywords: pancreatic cancer, PA-MSHA, cell cycle arrest, apoptosis, EGFR

Received: May 16, 2016    Accepted: October 14, 2016    Published: October 24, 2016


Pseudomonas aeruginosa-mannose-sensitive hemagglutinin (PA-MSHA) has demonstrated efficacy against several solid tumors. In this study, we found that PA-MSHA inhibited the proliferation of PANC-1 and SW1990 pancreatic cancer cells, but had no obvious effects on HPDE6-C7 normal human pancreatic duct epithelial cells. Electron microscopy revealed the presence of apoptotic bodies and intracellular vacuole formation in PA-MSHA-treated pancreatic cancer cells. Flow cytometric analysis indicated the rate of apoptosis correlated with the PA-MSHA concentration. We observed a decrease in cell fractions in G0/G1 and G2/M phases, and an increase in the fraction in S phase (p < 0.01). PA-MSHA thus caused cell cycle arrest. Increasing concentrations of PA-MSHA did not alter total levels of EGFR, AKT or ERK, but levels of the corresponding phosphoproteins decreased. PA-MSHA also reduced tumor volume in a xenograft mouse model of pancreatic cancer (p < 0.01). Furthermore, caspase-3 levels decreased while the levels of cleaved caspase-3 increased (p < 0.01). These data suggest that by blocking cell cycle progression, PA-MSHA induces apoptosis and inhibits tumor growth. PA-MSHA-mediated inhibition of EGFR signaling and activation of the caspase pathway may play an important role in the induction of apoptosis in pancreatic cancer cells.

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